Accidents, Traffic ; Early Diagnosis ; Female ; Fractures, Bone ; Humans ; Jeollanam-do ; Lacerations ; Male ; Mandibular Fractures ; Surgery, Oral

No abstract available.
Blood Glucose* ; Humans ; Infant, Newborn ; Infant, Premature*

In order to discover difference that may exist in quantity of medical care services, length of stay and hospital changes between insured and non-insured patients, records for primary Cesarean section patients discharged between July 1978 and June 1980 from a university hospital were examined. In addition, Cesarean section rates among the total deliveries for a two-year period between the groups were studied. The results showed that volume of services was greater and length of stay was longer among the insured, however, charges were higher among the non-insured. Cesarean section rates were statistically significantly different between insured and non-insured patients for every age group except the group of 35 or more.
Cesarean Section* ; Female ; Humans ; Length of Stay ; Pregnancy

OBJECTIVE: Moyamoya disease (MMD) is an uncommon cerebrovascular disorder, characterized by progressive occlusion at the terminal portion of the internal carotid artery. Incidence of the disease is high in East Asia and familial MMD accounts for about 15% of the disease. Although the pathogenesis is unknown, association of HLA class I or II alleles with MMD has been reported with conflicting results. We investigated whether there is a difference in HLA class II association between familial and non-familial forms of the disease. METHODS: A total of 70 Korean children with MMD, including 16 familial cases (10 probands), and 207 healthy controls were studied. Among familial cases, only 10 probands were used for the HLA frequency analysis. High resolution HLA-DRB1 and DQB1 genotyping was performed using polymerase chain reaction (PCR)-sequence specific oligonucleotide hybridization and PCR-single strand conformation polymorphism methods. RESULTS: The phenotype frequencies of HLA-DRB1*1302 (70.0%) and DQB1*0609 (40.0%) were significantly increased in familial MMD compared to both controls [vs. 15.5%, corrected p (pc) = 0.008, odds ratio (OR) = 12.76; vs. 4.3%, pc = 0.02, OR = 14.67] and non-familial MMD patients (vs. 14.8%, pc = 0.02, OR = 13.42; vs. 1.9%, pc = 0.02, OR = 35.33). The frequencies of DRB1 and DQB1 alleles in non-familial MMD patients were not significantly different from those in controls. CONCLUSION: Our findings suggest that the genetic polymorphism of HLA class II genes or other closely linked disease relevant gene(s) could be a genetic predisposing factor for familial MMD.
Alleles ; Carotid Artery, Internal ; Cerebrovascular Disorders ; Child ; Chimera ; Far East ; Genes, MHC Class II ; HLA-DQ Antigens ; HLA-DR Antigens ; HLA-DRB1 Chains ; Humans ; Incidence ; Moyamoya Disease ; Odds Ratio ; Phenotype ; Polymerase Chain Reaction ; Polymorphism, Genetic

We studied the angiographic findings in 65 patients wtih congenital pulmonary atresia, ages 4 days to 14 years(mean 3.3 yrs), form 1981 to 1986 at Severance Hospital Yonsei University. 1. 6 had pulmonary atresia with anintact interventricular septum, 38 had it with cardiac anomaly Renodynamically simulating TOF, and 21 associatedwith more complicated cardiac anomalies. 2. In the group with an intact ventricular septum, 5 showed confluentintrapericardial pulmonary artery, all segmental pulmonary arteries connceted to intrapericardial pulmoanryartery. 3. In the group simulating TOF, aorta arose from RV with or without overriding in 35. In 27 patients withconfluent intrapericardial pulmonary artery, 23 had more than 10 segmental pulmoanry arteries connceted tointrapericardial artery and 5 had severely hypoplastic hilar pulmonary arteries. In 11 with nonconfluentintrapericardial pulmonary artery, 4 had more than 10 segmental pulmonary arteries connected to central pulmonaryartery and 9 had severely hypoplastic hilar pulmonary arteries. 4. In the group associated with more complicatedcardiac anomaly, included 8 patients with atrioventricular discordance, 7 with univentricular heart and 6 withtricuspid atresia. In 17 patients with confluent intrapericardial artery, 16 had more than 10 segmental pulmoanryarteries conncected to intrapeircardial artery, one showed severe hypoplasia of hilar pulmonary arteries. Inanother 4 with nonconfluence, no one showed more than 10 segmental arteries conncted to intraperdicardial or hilarpulmonary artery.
Aorta ; Arteries ; Heart ; Humans ; Pulmonary Artery ; Pulmonary Atresia ; Ventricular Septum

PURPOSE: Insulin-like growth factor-I (IGF-I) is an important mitogen in many types of malignancies. The purpose of this study was to evaluate the role of the IGF system on cell proliferation and cell death in mouse lung cancer cell lines (3LL). MATERIALS AND METHODS: Northern analysis was performed in 3LL cells. We evaluated the phosphorylation of IGF-I receptor (IGF-IR) with IGF-I stimulation. MTT assay was performed after treating 3LL cells with IGF-I and the treatment effect on cell death in the presence of anticancer drug was investigated. RESULTS: Northern analysis revealed the presence of IGF-I and IGF-IR mRNA expression in 3LL cells. IGF-I increased cellular proliferation in serum free media. IGF-I also stimulated the tyrosine phosphorylation of two proteins: one, with a molecular mass of 95 kDa, was the beta-subunit of IGF-IR; the other, with an approximate molecular mass of 185 kDa, was originally identified as the insulin receptor substrate-I (IRS-I). IGF-I at a low concentration inhibited the cell death induced by adriamycin. CONCLUSION: IGF-I, a mitogen through the phosphorylation of the IGF-IR beta-subunit, acts as a survival factor to inhibit cell death. Therefore, these findings suggest that IGF-I and IGF-IR are involved in both the cell proliferation and cell death associated with cancer cell growth.
Animals ; Cell Death ; Cell Line ; Cell Proliferation ; Culture Media, Serum-Free ; Doxorubicin ; Insulin-Like Growth Factor I ; Lung Neoplasms* ; Lung* ; Mice* ; Phosphorylation ; Receptor, IGF Type 1 ; Receptor, Insulin ; RNA, Messenger ; Tyrosine

No abstract available.

BACKGROUND: IGF-I is an important mitogen in many types of malignancies. Tumors also express many IGF binding proteins, which modulate IGF action. The purpose of this study was to evaluaste the effect of IGF-I and IGFBP on cell proliferation in mouse lung cancer cells (3LL). METHODS: The cellular proliferation of 3LL with the treatment of growth factors was evaluated using MTT assay. Western ligand blot was performed in order to determine whether 3LL cells secrete IGFBPs and we evaluated the effect of IGFBP on cellular proliferation. RESULTS: The treatment of 3LL cells with IGF-I increased cellular proliferation in a serum free media. Western ligand blot of conditioned medium of 3LL with 125I-IGF-I demonstrated one single major band with an estimated molecular mass of 24 kDa. This band was identified as IGFBP-4 with immunoblot analysis using antisera. The addition of anti-IGFBP-4 antibody to abrogate the effect of IGFBP-4 resulted in increased cellular prolife ration suggesting that IGFBP-4 inhibits cell growth. CONCLUSION: IGF-I increases cellular proliferation, however the secreted IGFBP- 4 has an ingibitory function on cell growth in 3LL. These findings suggest that IGF-I and IGFBP are involved in the cell proliferation.
Animals ; Carrier Proteins* ; Cell Proliferation ; Culture Media, Conditioned ; Culture Media, Serum-Free ; Immune Sera ; Insulin-Like Growth Factor Binding Protein 4 ; Insulin-Like Growth Factor Binding Proteins ; Insulin-Like Growth Factor I ; Intercellular Signaling Peptides and Proteins ; Lung Neoplasms* ; Lung* ; Mice*

The Mayer-Rokitansky-K ster-Hauser syndrome represents a spectrum of m llerian anomalies, including vaginal agenesis with or without renal anomalies, in genotypically and phenotypically normal female subjects with normal endocrine status. We experienced a case of this anomaly which combined with unilateral renal agenesis and pelvic cystic mass in child.
Child* ; Female ; Humans

No abstract available.
Humans ; Pulmonary Atresia* ; Siblings* ; Ventricular Septum*